Current perspectives of molecular pathways involved in chronic inflammation-mediated breast cancer

Suman, Shankar; Sharma, Pradeep K.; Rai, Girish; Mishra, Sanjay; Arora, Deepika; Gupta, Prachi; Shukla, Yogeshwer

doi:10.1016/j.bbrc.2015.10.133

Cited by 53 publications

(30 citation statements)

References 125 publications

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“…Other cytokines, chemokines and growth factors may also promote cancer-associated inflammation and metastasis inhibiting certain biological processes as the imbalance of oxidative stress, autophagy and angiogenesis 40 . Furthermore, CAFs can recruit immune cells responsible for the secretion of pro-inflammatory molecules, which contribute to tumor progression triggering immunosuppressive or ineffective host-antitumor responses 41 .…”

Section: Discussionmentioning

confidence: 99%

GPER signalling in both cancer-associated fibroblasts and breast cancer cells mediates a feedforward IL1β/IL1R1 response

Marco

Lappano

Francesco

et al. 2016

Sci Rep

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Cancer-associated fibroblasts (CAFs) contribute to the malignant aggressiveness through secreted factors like IL1β, which may drive pro-tumorigenic inflammatory phenotypes mainly acting via the cognate receptor named IL1R1. Here, we demonstrate that signalling mediated by the G protein estrogen receptor (GPER) triggers IL1β and IL1R1 expression in CAFs and breast cancer cells, respectively. Thereby, ligand-activation of GPER generates a feedforward loop coupling IL1β induction by CAFs to IL1R1 expression by cancer cells, promoting the up-regulation of IL1β/IL1R1 target genes such as PTGES, COX2, RAGE and ABCG2. This regulatory interaction between the two cell types induces migration and invasive features in breast cancer cells including fibroblastoid cytoarchitecture and F-actin reorganization. A better understanding of the mechanisms involved in the regulation of pro-inflammatory cytokines by GPER-integrated estrogen signals may be useful to target these stroma-cancer interactions.

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Section: Discussionmentioning

confidence: 99%

GPER signalling in both cancer-associated fibroblasts and breast cancer cells mediates a feedforward IL1β/IL1R1 response

Marco

Lappano

Francesco

et al. 2016

Sci Rep

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“…Similarly, Wulaningsih et al suggested that CRP was associated with mortality from breast cancer [21]. A chronic inflammatory related to obesity can cause oxidative damage and inactivate proteins involved in DNA repair or apoptotic control, resulting in cancer cell initiation and growth [22]. These studies prompted that poor prognosis of obese breast cancer patients was partly due to inflammation induced by obesity.…”

Section: Discussionmentioning

confidence: 99%

Association of 15-hydroxyprostaglandin dehydrogenate and poor prognosis of obese breast cancer patients

Liu

Yang

et al. 2017

Oncotarget

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In order to explore the new mechanism that obesity worsens the prognosis of breast cancer, we reanalyzed the data about gene expression of normal, overweight, and obese breast cancer patients to explore potential genes and validate its function by clinical and experimental data. The fold change of 15-hydroxyprostaglandin dehydrogenate (HPGD) gene which displayed declining trend with BMI increase was 0.46 in obese versus normal weight patients. HPGD protein was highest expressed in normal weight group and lowest expressed in obese group. The rate of positive lymph nodes was 67% in low expression of HPGD group and 35% in high expression of HPGD group. The recurrence-free survival (RFS) rate and overall survival (OS) rate of 5 years had significant difference between low expression of HPGD group and high expression of HPGD group. Obesity dramatically decreased the RFS rate and OS rate of 5 years. Down regulation of HPGD expression could increase the migration and proliferation ability of breast cancer cell line MCF-7. Taken together, our results indicate that low expression of HPGD may be a reason for poor prognosis of obese breast cancer patients.

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“…In addition, there is a high correlation between autophagy, inflammation and tumor [ 10 – 13 ]. Autophagy is a self-protective mechanism to maintain homestasis by breaking down the intracellular impaired protein or organelles, and it is considered as a two-edge sword having both anti- and pro-tumor functions at different stages of tumor development [ 14 , 15 ], and more and more new insights strongly indicate that autophagy not only plays its classical role as a house-keeping mechanism, but also can be considered as crucial for induction and modulation of inflammatory reaction [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Ethanol extract of propolis and its constituent caffeic acid phenethyl ester inhibit breast cancer cells proliferation in inflammatory microenvironment by inhibiting TLR4 signal pathway and inducing apoptosis and autophagy

Chang

Wang

Yin

et al. 2017

BMC Complement Altern Med

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BackgroundPropolis and its major constituent – caffeic acid phenethyl ester (CAPE) have good abilities on antitumor and anti-inflammation. However, little is known about the actions of propolis and CAPE on tumor in inflammatory microenvironment, and inflammatory responses play decisive roles at different stages of tumor development. To understand the effects and mechanisms of ethanol-extracted Chinese propolis (EECP) and its major constituent - CAPE in inflammation-stimulated tumor, we investigated their effects on Toll-like receptor 4 (TLR4) signaling pathway which plays a crucial role in breast cancer MDA-MB-231 cell line.Methods80% confluent breast cancer MDA-MB-231 cells were stimulated with 1 μg/mL lipopolysaccaride (LPS). Then the cells were divided for treatment by CAPE (25 μg/mL) and EECP (25, 50 and 100 μg/mL), respectively. Cell viability, nitric oxide (NO) production and cell migration were measured by sulforhodamine B assay, chemical method and scratch assay. The levels of TLR4, MyD88, IRAK4, TRIF, caspase 3, PARP, LC3B and p62 were investigated through western blotting. The expression of TLR4, LC3B and nuclear factor-κB p65 (NF-κB p65) were tested by immunofluorescence microscopy assay.ResultsTreatment of different concentrations of EECP (25, 50 and 100 μg/mL) and CAPE (25 μg/mL) significantly inhibited LPS-stimulated MDA-MB-231 cell line proliferation, migration and NO production. Furthermore, EECP and CAPE activated caspase3 and PARP to induce cell apoptosis, and also upregulated LC3-II and decreased p62 level to induce autophagy during the process. TLR4 signaling pathway molecules such as TLR4, MyD88, IRAK4, TRIF and NF-κB p65 were all down-regulated after EECP and CAPE treatment in LPS-stimulated MDA-MB-231 cells.ConclusionsThese findings indicated that EECP and its major constituent - CAPE inhibited breast cancer MDA-MB-231 cells proliferation in inflammatory microenvironment through activating apoptosis, autophagy and inhibiting TLR4 signaling pathway. EECP and CAPE may hold promising prospects in treating inflammation-induced tumor.

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Current perspectives of molecular pathways involved in chronic inflammation-mediated breast cancer

Cited by 53 publications

References 125 publications

GPER signalling in both cancer-associated fibroblasts and breast cancer cells mediates a feedforward IL1β/IL1R1 response

GPER signalling in both cancer-associated fibroblasts and breast cancer cells mediates a feedforward IL1β/IL1R1 response

Association of 15-hydroxyprostaglandin dehydrogenate and poor prognosis of obese breast cancer patients

Ethanol extract of propolis and its constituent caffeic acid phenethyl ester inhibit breast cancer cells proliferation in inflammatory microenvironment by inhibiting TLR4 signal pathway and inducing apoptosis and autophagy

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